Many frugivorous avian species kept in captivity develop iron storage disease (ISD) as indicated by high concentrations of hepatic iron and hemosiderin deposits in hepatocytes or phagocytes. In several susceptible species fed diets containing moderate levels of iron, ISD develops because of an inability to match rates of iron absorption to tissue needs. Evidence suggests that the pathophysiologic basis of excess iron absorption is due to high levels of expression of divalent metal transporter-1 that transports iron into enterocytes in the proximal intestine, and ferroportin that exports iron to the circulation. The regulatory basis for this inability to sufficiently down-regulate iron absorption is unknown, but disruptions in the hepcidin–ferroportin axis are likely candidates based on recent research in humans and laboratory rodents. It is likely that ISD-susceptible avian species evolved on foods that were very low in bioavailable iron, so there was strong selection pressure for the efficient capture of the small amount of dietary iron but low selection pressure for preventing iron toxicities. Thus, the transporters and regulatory networks for iron absorption seem to be heavily skewed toward iron storage even when food items that are high in iron are consumed. Infections, trauma and neoplasias that trigger an acute phase response may exacerbate ISD in susceptible species and may be the primary cause in species that are normally resistant to ISD (i.e., those that are normally able to shut down intestinal iron absorption when iron stores are replete). The evolutionary basis that resulted in some avian species to be susceptible to ISD (e.g., dietary cause) seems to differ from many inherited ISD disorders in humans that are thought to have evolved to bolster protection against infectious diseases. However the evolutionary basis of ISD in other mammalian species might be more similar to that in ISD-susceptible avian species.
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